Most carcinogens or their metabolic products have a variety of features in common: they can combine with DNA, the lesions can be repaired by cellular repair processes, and the carcinogens are also mutagens. In bacteria, the mutations are the result of an inducible, error-prone, DNA repair system (SOS repair). Our main objective is to study the relationship between mutagenesis, carcinogenesis, and DNA repair in animal cells. Error-prone DNA repair pathways in animal cells exposed to UV light and chemical carcinogens will be identified and the genetic, physiological and pharmacological factors which control these processes shall be ascertained. The effects of heavy metals on DNA repair in E. coli shall be studied, as well as the role of proteases in error-prone repair. Using Chinese hamster ovary cell, a series of DNA-repair-deficient mutants will be isolated, which will allow analysis of the various DNA repair pathways. Error-prone repair will be measured as the mutation frequency, using ouabain resistance as a marker, in cells exposed to a known UV fluence. It is hoped that this system will be useful as a screen for both carcinogens and co-carcinogens. BIBLIOGRAPHIC REFERENCES: Rossman, T.G., Meyn, M.S. and TRoll, W. Effects of Arsenite on DNA Repair in Escherichia coli. Environ. Health Perspectives, 1977, in press. Rossman, T., Lustig, D., and Troll, W. Evidence for an Inducible DNA-repair System in Animal Cells (abs.) In Vitro 1977, in press.